Fig. 2: B3galt5 is a direct transcriptional target gene of PXR.

a Heat map representation of genes deferentially expressed in the intestine of 8-week-old mice treated with vehicle (Veh) and PCN. Mice were treated with PCN (40 mg/kg) once every 8 hours for three times (n = 2 per group). b Intestinal mRNA expression of B3galt5 in WT mice treated with PXR agonists PCN and TBC (n = 8 for Veh, n = 10 for PCN, n = 8 for Veh, n = 8 for TBC). Significance was determined using unpaired two-tailed Student’s t test. c Intestinal mRNA expression of B3galt5 in PXR knockout mice treated with PCN and TBC (n = 5 for Veh, n = 4 for PCN, n = 6 for Veh, n = 7 for TBC). d Intestinal protein level of B3galt5 in WT and PXR knockout mice treated with TBC, β-Tubulin was used as the loading control. e Electrophoretic mobility shift assay (EMSA) showing that PXR binds to the −1793 to −1814 region of B3galt5 promoter. f Luciferase assay of HEK293 cells co-transfected with B3galt5 or mutant B3galt5 and treated with PCN for 24 h. The luciferase activity was normalized to β-gal (n = 3 per group). g ChIP assay of recruitment of PXR to the B3galt5 promoter (n = 3 per group). h, i The mRNA expression of B3galt5 (h) and MDR1 (i) in LS174T cells treated with TBC (5 μM) or rifampicin (RIF, 20 μM) for 48 h (n = 3 per group). j The protein levels of B3galt5 in LS174T cells treated with TBC or RIF, β-Tubulin was used as the loading control. Data are mean ± SEM. PXR KO PXR whole-body knockout mice, WT wild type, TBC tributyl citrate, ChIP chromatin immunoprecipitation, RIF rifampicin. The data sets (Fig. 1f-i) were analyzed using non-parametric approaches and the statistical differences between groups were determined using one-way ANOVA with post-hoc Tukey test. Source data are provided as a Source Data file.